Heart-specific inducible CAR knockout impaired electrical conduction between atrium and ventricle due to altered expression and localization of connexins.
Does the loss of the Coxsackievirus-adenovirus receptor (CAR) impair cardiac conduction and cell-cell communication in the adult heart?
CAR has a previously unknown function in atrioventricular excitation propagation, which may explain the association between Coxsackievirus infection and cardiac arrhythmias.
The Coxsackievirus-adenovirus receptor (CAR) is known for its role in virus uptake and as a protein of the tight junction. It is predominantly expressed in the developing brain and heart and reinduced upon cardiac remodeling in heart disease. So far, the physiological functions of CAR in the adult heart are largely unknown. We have generated a heart-specific inducible CAR knockout (KO) and found impaired electrical conduction between atrium and ventricle that increased with progressive loss of CAR. The underlying mechanism relates to the cross talk of tight and gap junctions with altered expression and localization of connexins that affect communication between CAR KO cardiomyocytes. Our results indicate that CAR is not only relevant for virus uptake and cardiac remodeling but also has a previously unknown function in the propagation of excitation from the atrium to the ventricle that could explain the association of arrhythmia and Coxsackievirus infection of the heart.
Lisewski et al. (Mon,) conducted a other in Cardiac conduction and cell-cell communication. Heart-specific inducible CAR knockout was evaluated on Electrical conduction between atrium and ventricle. Heart-specific inducible CAR knockout impaired electrical conduction between atrium and ventricle due to altered expression and localization of connexins.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: